Chemical Property of Iniparib
Chemical Property:
- Vapor Pressure:0mmHg at 25°C
- Refractive Index:1.696
- Boiling Point:344.754 °C at 760 mmHg
- PKA:14?+-.0.50(Predicted)
- Flash Point:162.302 °C
- PSA：88.91000
- Density:2.056 g/cm3
- LogP:2.52180
- Storage Temp.:room temp
- Solubility.:DMSO: soluble5mg/mL, clear
- XLogP3:1.3
- Hydrogen Bond Donor Count:1
- Hydrogen Bond Acceptor Count:3
- Rotatable Bond Count:1
- Exact Mass:291.93449
- Heavy Atom Count:13
- Complexity:228
- Purity/Quality:
-
97% *data from raw suppliers
Iniparib *data from reagent suppliers
Safty Information:
- Pictogram(s):
Xn
- Hazard Codes:Xn
- Statements:
22-36-43
- Safety Statements:
26
- MSDS Files:
-
SDS file from LookChem
Useful:
- Canonical SMILES:C1=CC(=C(C=C1C(=O)N)[N+](=O)[O-])I
- Recent ClinicalTrials:Treatment Extension Study for Patients Who Have Previously Participated and Have Benefited From Iniparib in a Clinical Trial
- Recent EU Clinical Trials:International, Multi-Center, Open-label, Treatment Extension Study of Iniparib as Monotherapy or in Combination Chemotherapeutic Regimens in Cancer Patients Who Have Derived Clinical Benefit From Iniparib Following Completion of a Phase 1, 2 or 3 Parental Study
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Description
Iniparib (160003-66-7) was originally thought to be a PARP1 inhibitor but this is controversial.1,2?Inhibits ionizing radiation-induced single-stranded DNA break repair in lymphoid cell lines?in vivo.3?Inhibits growth of certain breast cancer cell lines?in vitro. Iniparib non-selectively modifies cysteine-containing proteins in tumor cells.4
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Uses
Iniparib is an irreversible PARP1 inhibitor. Studies show that potential therapeutic agent for the treatment of cancer, including triple-negative breast cancer. Iniparib (BSI-201) is an antineoplastic originally thought to be a poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor. Recent studies indicate Iniparib is not a PARP-1 inhibitor, and its mechanism of action is currently unknown. Poly(ADP-ribose) polymerase (PARP) is a critical DNA repair enzyme involved in DNA single-strand break repair via the base excision repair pathway. PARP1 is activated by DNA damage. Inhibiting its activity has been linked to synthetic lethality and loss of either of the breast cancer susceptibility genes, BRCA1 and BRCA2. BSI-201 is an irreversible, noncompetitive inhibitor of PARP1 that disrupts binding between PARP1 and DNA by interacting with the DNA binding domain. It produces rapid apoptosis in various cancer cell lines with IC50 values ranging from 40-128 μM and is not toxic in Syrian hamsters at doses as high as 200 mg/kg. In phase II clinical studies, BSI-201, in combination with carboplatin and gemcitabine, has produced promising results in "triple-negative" breast cancers, increasing median overall survival from 7.7 months to 12.3 months.
